Veterinary Sciences,
Journal Year:
2024,
Volume and Issue:
11(2), P. 77 - 77
Published: Feb. 7, 2024
Equine
melanocytic
tumors
are
common
and
have
an
unusual
benign
behavior
with
low
invasiveness
metastatic
rates.
However,
tumoral
mass
growth
is
usually
a
concern
that
can
life-threatening
consequences.
COX-2
related
to
oncogenesis,
promoting
neoplastic
cell
proliferation,
invasion,
metastasis.
The
aim
of
this
study
was
evaluate
the
immunohistochemical
expression
in
equine
tumors.
Through
extension
intensity
labeling,
39
melanocytomas
38
melanomas
were
evaluated.
Of
malignant
tumors,
13.2%
negative
63.2%
presented
expression.
Only
6
>50%
labeled
cells,
18
8
had
between
21
50%,
3
20%,
1
tumor
5%,
5
28
no
Malignant
showed
higher
than
did
statistically
significant
differences.
levels
may
be
one
molecular
reasons
for
presence
expansive
instead
invasive
pattern
other
species,
which
high
levels.
Cancers,
Journal Year:
2023,
Volume and Issue:
15(16), P. 4026 - 4026
Published: Aug. 8, 2023
Melanoma
is
an
aggressive
form
of
skin
cancer
resulting
from
the
malignant
transformation
melanocytes.
Recent
therapeutic
approaches,
including
targeted
therapy
and
immunotherapy,
have
improved
prognosis
outcome
melanoma
patients.
BRAF
one
most
frequently
mutated
oncogenes
recognised
in
melanoma.
The
frequent
oncogenic
mutations
consist
a
single
point
mutation
at
codon
600
(mostly
V600E)
that
leads
to
constitutive
activation
BRAF/MEK/ERK
(MAPK)
signalling
pathway.
Therefore,
has
become
useful
target
for
molecular
use
kinase
inhibitors
shown
promising
results.
However,
several
resistance
mechanisms
invariably
develop
leading
failure.
aim
this
manuscript
review
role
mutational
status
pathogenesis
its
impact
on
differentiation
inflammation.
Moreover,
focuses
responsible
therapies
BRAF-mutated
provides
overview
circulating
biomarkers
tumour
cells,
DNA,
non-coding
RNAs.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(5), P. 2984 - 2984
Published: March 4, 2024
Melanoma,
a
highly
aggressive
skin
cancer,
is
characterized
by
rapid
progression
and
high
mortality.
Recent
advances
in
molecular
pathogenesis
have
shed
light
on
genetic
epigenetic
changes
that
drive
melanoma
development.
This
review
provides
an
overview
of
these
developments,
focusing
mechanisms
genesis.
It
highlights
how
mutations,
particularly
the
BRAF,
NRAS,
c-KIT,
GNAQ/GNA11
genes,
affect
critical
signaling
pathways.
The
evolution
diagnostic
techniques,
such
as
genomics,
transcriptomics,
liquid
biopsies,
biomarkers
for
early
detection
prognosis,
also
discussed.
therapeutic
landscape
has
transformed
with
targeted
therapies
immunotherapies,
improving
patient
outcomes.
paper
examines
efficacy,
challenges,
prospects
treatments,
including
recent
clinical
trials
emerging
strategies.
potential
novel
treatment
strategies,
neoantigen
vaccines,
adoptive
cell
transfer,
microbiome
interactions,
nanoparticle-based
combination
therapy,
explored.
These
emphasize
challenges
therapy
resistance
importance
personalized
medicine.
underlines
necessity
evidence-based
selection
managing
increasing
global
incidence
melanoma.
Cancers,
Journal Year:
2024,
Volume and Issue:
16(2), P. 470 - 470
Published: Jan. 22, 2024
Melanoma
is
the
third
most
common
type
of
skin
cancer,
characterized
by
its
heterogeneity
and
propensity
to
metastasize
distant
organs.
a
heterogeneous
tumor,
composed
genetically
divergent
subpopulations,
including
small
fraction
melanoma-initiating
cancer
stem-like
cells
(CSCs)
many
non-cancer
stem
(non-CSCs).
CSCs
are
their
unique
surface
proteins
associated
with
aberrant
signaling
pathways
causal
or
consequential
relationship
tumor
progression,
drug
resistance,
recurrence.
Melanomas
also
harbor
significant
alterations
in
functional
genes
(BRAF,
CDKN2A,
NRAS,
TP53,
NF1).
Of
these,
BRAF
NRAS
oncogenes,
50%
melanomas
demonstrating
mutation
(BRAF
Cancers,
Journal Year:
2024,
Volume and Issue:
16(5), P. 913 - 913
Published: Feb. 23, 2024
Melanoma
progression
is
a
multistep
evolution
from
common
melanocytic
nevus
through
radial
superficial
growth
phase,
the
invasive
vertical
phase
finally
leading
to
metastatic
dissemination
into
distant
organs.
aggressiveness
largely
depends
on
propensity
metastasize,
which
means
capacity
escape
physiological
microenvironment
since
tissue
damage
due
primary
melanoma
lesions
generally
modest.
Physiologically,
epidermal
melanocytes
are
attached
basement
membrane,
and
their
adhesion/migration
under
control
of
surrounding
keratinocytes.
Thus,
compartment
represents
first
responsible
for
spread.
This
complex
process
involves
cell-cell
contact
broad
range
secreted
bioactive
molecules.
Invasion,
or
at
beginning
microinvasion,
implies
breakdown
dermo-epidermal
membrane
followed
by
migration
neoplastic
cells
in
papillary
dermis.
Correspondingly,
several
experimental
evidences
documented
structural
functional
rearrangement
entire
neoplasm
that
some
way
reflects
atypia
tumor
cells.
Lastly,
must
support
proliferation
survival
outside
normal
epidermal-melanin
units.
task
presumably
mostly
delegated
fibroblasts
ultimately
self-autonomous
review
will
discuss
remodeling
occurs
epidermis
during
formation
as
well
skin
changes
occur
independently
hyperproliferation
having
possible
pro-tumoral
features.
Cells,
Journal Year:
2024,
Volume and Issue:
13(3), P. 240 - 240
Published: Jan. 26, 2024
Melanoma
frequently
harbors
genetic
alterations
in
key
molecules
leading
to
the
aberrant
activation
of
PI3K
and
its
downstream
pathways.
Although
role
PI3K/AKT/mTOR
melanoma
progression
drug
resistance
is
well
documented,
targeting
pathway
showed
less
efficiency
clinical
trials
than
might
have
been
expected,
since
suppression
PI3K/mTOR
signaling
pathway-induced
feedback
loops
mostly
associated
with
compensatory
pathways
such
as
MAPK/MEK/ERK.
Consequently,
development
intrinsic
acquired
can
occur.
As
a
solid
tumor,
notorious
for
heterogeneity.
This
be
expressed
form
genetically
divergent
subpopulations
including
small
fraction
cancer
stem-like
cells
(CSCs)
non-cancer
stem
(non-CSCs)
that
make
most
tumor
mass.
Like
other
CSCs,
(MSCs)
are
characterized
by
their
unique
cell
surface
proteins/stemness
markers
In
addition
function
robust
marker
stemness
properties,
CD133
crucial
maintenance
properties
resistance.
Herein,
CD133-dependent
regulation
progression,
resistance,
recurrence
reviewed.
Biomedicine & Pharmacotherapy,
Journal Year:
2024,
Volume and Issue:
177, P. 116953 - 116953
Published: July 1, 2024
The
second
most
common
mutation
in
melanoma
occurs
NRAS
oncogene,
being
a
more
aggressive
disease
that
has
no
effective
approved
treatment.
Besides,
cellular
plasticity
limits
better
outcomes
of
the
advanced
and
therapy-resistant
patients.
Peroxiredoxins
(PRDXs)
control
processes
through
direct
hydrogen
peroxide
oxidation
or
by
redox-relaying
processes.
Here,
we
demonstrated
PRDX2
could
act
as
modulator
multiple
EMT
markers
NRAS-mutated
melanomas.
knockdown
lead
to
phenotypic
changes
towards
invasion
human
reconstructed
skin
treatment
with
PRDX
mimetic
(gliotoxin),
decreased
migration
PRDX2-deficient
cells.
We
also
confirmed
favorable
clinical
outcome
patients
expressing
large
primary
cohort.
This
study
contributes
our
knowledge
about
genes
involved
phenotype
switching
opens
new
perspective
for
biomarker
target
Biomedicines,
Journal Year:
2025,
Volume and Issue:
13(1), P. 225 - 225
Published: Jan. 17, 2025
Malignant
melanoma
(MM)
is
a
malignant
tumor,
resulting
from
mutations
in
melanocytes
of
the
skin
and
mucous
membranes.
Its
mortality
rate
accounts
for
90%
all
dermatologic
tumor
mortality.
Traditional
treatments
such
as
surgery,
chemotherapy,
radiotherapy
are
unable
to
achieve
expected
results
due
MM's
low
sensitivity,
high
drug
resistance,
toxic
side
effects.
As
treatment
advances,
immunotherapy
targeted
therapy
have
made
significant
breakthroughs
MM
demonstrated
promising
application
prospects.
However,
heterogeneity
immune
response
causes
more
than
half
patients
not
benefit
clinical
therapy,
which
delays
patient's
condition
them
suffer
adverse
events'
The
combination
can
help
improve
therapeutic
effects,
delay
mitigate
This
review
provides
comprehensive
overview
current
development
status
research
progress
checkpoints,
genes,
their
inhibitors,
with
view
providing
reference
MM.